During this period we conducted a number of studies of the role of IL-5 and other lymphokines in B cell differentiation, particularly IgA B cell differentiation. In one set of studies we performed an extensive evaluation of IL-5 receptor (lL-5R) expression on B cell lines and on stimulated normal B cells. We found that IL-5 binds to a high affinity and low affinity receptor on the B cell surface. Stimulation of normal B cells with alpha-delta-dextran, greatly augments high affinity IL-5R expression, whereas alpha-mu antibody or PMA/Ionomycin causes only minimal increases in IL-5R expression. In addition, LPS does not increase IL-5R expression and inhibits that induced by alpha-delta-dextran. These results indicate that IL-5R expression on B cells requires activation of the latter with agents that extensively cross-link surface Ig. In addition, they suggest that certain bacterial surface components may act to down-regulate immune responses by inhibiting lL-5R expression. In other studies, we continued to explore the effect of IL-5 and other lymphokines of B cell differentiation. We induced antigen-specific B cell responses in Peyer's patches by oral administration of mice with inactivated influenza virus and cholera toxin adjuvant. We then determined the capacity of the induced IgA B cells to undergo terminal differentiation in vivo, in the presence of antigen and various lymphokines. We found that IL-5 and IFN-gamma could both act as independent terminal differentiation factors for IgA B cells and that these substances together gave additive effects. The highest IgA responses were obtained, however, with IL-4, IL-5 and IFNgamma. These results indicate that combinations of lymphokines are necessary to achieve maximal IgA B cell differentiation. Finally, we continued studies of the mechanism of action of cholera toxin on B cell responses. In these studies we determined the effect of cholera toxin (CT) on purified B cells stimulated either with LPS-alone or LPS plus IL-4. We found that CT induces preferential differentiation of IgG1 B cells and augments IL-4 induced IgG1 B cell differentiation. In addition, we found that CT induced gamma1 germline mRNA transcripts and augments gamma1 germline mRNA transcripts induced by IL-4. These studies indicate that CT acts to induce IgG1 at the level of isotype switching.